Silencing lncRNA 93358 Inhibits the Apoptosis of Myocardial Cells in Myocardial Infarction Rats by Inducing the

Jiumei Cai1,2,3, Xiaoping Wang2, Wei Liao2

  • 1The Second School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong 510515, China.

Abstract

Insights

Silencing long non-coding RNA 93358 (lncRNA 93358) inhibits myocardial cell apoptosis in myocardial infarction (MI) rat models. This protective effect is mediated by inducing the expression of solute carrier family 8 member A1 (SLC8A1).

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • RNA Biology

Background:

  • Myocardial infarction (MI) is a leading cause of mortality.
  • Apoptosis of myocardial cells exacerbates cardiac dysfunction post-MI.
  • Identifying novel therapeutic targets to mitigate myocardial cell death is crucial.

Purpose of the Study:

  • To investigate the inhibitory effects and mechanism of long non-coding RNA 93358 (lncRNA 93358) on myocardial cell apoptosis in a rat model of myocardial infarction.
  • To elucidate the role of lncRNA 93358 in regulating cell death pathways and its potential as a therapeutic target.

Main Methods:

  • Establishment of a rat model of myocardial infarction, confirmed by echocardiography.
  • Assessment of infarct size and myocardial pathology using TTC and HE staining.
  • Evaluation of myocardial cell apoptosis via TUNEL assay.
  • Identification and validation of lncRNA 93358 expression using high-throughput sequencing and RT-qPCR.
  • Investigation of the interaction between lncRNA 93358, miR-466c-3p, and SLC8A1 using dual-luciferase reporter assays.
  • Analysis of apoptosis-related protein and SLC8A1 expression (Bax, Bcl-2, SLC8A1) through RT-qPCR and Western blotting following lncRNA 93358 knockdown.

Main Results:

  • Myocardial infarction model rats exhibited significant myocardial necrosis, increased lncRNA 93358 and Bax expression, and decreased Bcl-2 and SLC8A1 levels.
  • Knockdown of lncRNA 93358 significantly reversed these changes, reducing infarct size and myocardial apoptosis.
  • lncRNA 93358 knockdown led to increased SLC8A1 expression, suggesting its role in the protective mechanism.

Conclusions:

  • Silencing lncRNA 93358 demonstrates a protective effect against myocardial cell apoptosis in a rat model of myocardial infarction.
  • The mechanism involves the induction of solute carrier family 8 member A1 (SLC8A1) expression.
  • lncRNA 93358 represents a potential therapeutic target for managing myocardial infarction by inhibiting apoptosis.

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